Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS024380-09
Application #
2265198
Study Section
Biochemistry Study Section (BIO)
Project Start
1987-02-01
Project End
1999-03-31
Budget Start
1996-04-01
Budget End
1997-03-31
Support Year
9
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Rosalind Franklin University
Department
Biochemistry
Type
Schools of Medicine
DUNS #
069501252
City
North Chicago
State
IL
Country
United States
Zip Code
60064
Mehta, Hrishikesh M; Woo, Sang B; Neet, Kenneth E (2012) Comparison of nerve growth factor receptor binding models using heterodimeric muteins. J Neurosci Res 90:2259-71
Bai, Yujing; Dergham, Pauline; Nedev, Hinyu et al. (2010) Chronic and acute models of retinal neurodegeneration TrkA activity are neuroprotective whereas p75NTR activity is neurotoxic through a paracrine mechanism. J Biol Chem 285:39392-400
Rogers, Mary-Louise; Bailey, Sheree; Matusica, Dusan et al. (2010) ProNGF mediates death of Natural Killer cells through activation of the p75NTR-sortilin complex. J Neuroimmunol 226:93-103
Masoudi, Raheleh; Ioannou, Maria S; Coughlin, Michael D et al. (2009) Biological activity of nerve growth factor precursor is dependent upon relative levels of its receptors. J Biol Chem 284:18424-33
Mahapatra, Sidharth; Mehta, Hrishikesh; Woo, Sang B et al. (2009) Identification of critical residues within the conserved and specificity patches of nerve growth factor leading to survival or differentiation. J Biol Chem 284:33600-13
Boutilier, Jacqueline; Ceni, Claire; Pagdala, Promila C et al. (2008) Proneurotrophins require endocytosis and intracellular proteolysis to induce TrkA activation. J Biol Chem 283:12709-16
Ivanisevic, Ljubica; Zheng, WenHua; Woo, Sang B et al. (2007) TrkA receptor ""hot spots"" for binding of NT-3 as a heterologous ligand. J Biol Chem 282:16754-63
Pagadala, Promila C; Dvorak, Laura A; Neet, Kenneth E (2006) Construction of a mutated pro-nerve growth factor resistant to degradation and suitable for biophysical and cellular utilization. Proc Natl Acad Sci U S A 103:17939-43
Vaghefi, Houman; Neet, Kenneth E (2004) Deacetylation of p53 after nerve growth factor treatment in PC12 cells as a post-translational modification mechanism of neurotrophin-induced tumor suppressor activation. Oncogene 23:8078-87
Vaghefi, Houman; Hughes, Allison L; Neet, Kenneth E (2004) Nerve growth factor withdrawal-mediated apoptosis in naive and differentiated PC12 cells through p53/caspase-3-dependent and -independent pathways. J Biol Chem 279:15604-14

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